Abstract:

To study the effect of ginsenoside Rb3 (G-Rb₃) on experimental ventricular remodeling  in rats and investigate its mechanism.  Methods The ventricular remodeling model was induced by myocardial infarction in rats of left anterior descending coronary occulusion. The Wistar rats were divided into 4 groups:sham operation group,remodeling model group,G-Rb3 group,and captopril group. The rats in sham operation group and remodeling model group were treated with normal sodium (with 2mL·kg^-1·d^-1 i.p).The rats in G-Rb₃ group were treated with G-Rb₃ (with 20 mg·kg^-1·d^-1 i.p). The rats in captopril group was treated with captopril (100 mg·kg^-1·d^-1 i.g). After 4 weeks,the morphological parameters,histopathology,hemodynamic changes,biochemical analysis were determined in rats. The content of malondialdehyde (MDA) in serum and activities of superoxide dismutase(SOD),glutathione  peroxidase (GSH-Px) in plasma,the content of endothelin (ET),angiotensin Ⅱ(AngⅡ) in plasma,myocardial angiotensin Ⅱ(AngⅡ) were determined.  Results Compared with model group,the cardiac coefficient,the left ventricular end diastolic pressure (LVEDP) were decreased significantly(P<0.01),the mean arterial blood pressure(MAP) and the maximum left ventricular presure rising and dropping rates (±dp/dtmax) were increased significantly in G-Rb₃ group(P<0.01). In addition,Compared with model group,the contents of MDA in serum,ET,AngⅡ in plasma and myocardial  AngⅡ were declined(P<0.01),then the activities of SOD and GSH-Px in serum were increased markedly in G-Rb₃group(P<0.01).  Conclusion G-Rb₃ has protective effect on ventricular remodeling through inhibitting renin-angiotensin-aldosterone system(RAAS) to reduce contractive material and  reinforcing  ability of anti-oxidant

Key words: G-Rb₃;myocardial infarction;ventricular remodeling;rats,Wistar